lignans and gamma-cyclodextrin

A facile method for the activation of γ-cyclodextrin metal-organic framework (CD-MOF) without channel blockage and framework collapse was first developed using supercritical carbon dioxide (scCO

Topics: Animals; Biological Availability; Biphenyl Compounds; Caco-2 Cells; Carbon Dioxide; Drug Delivery Systems; Fluorescent Dyes; gamma-Cyclodextrins; Humans; Hydrogen-Ion Concentration; Lignans; Male; Metal-Organic Frameworks; Molecular Structure; Optical Imaging; Particle Size; Rats; Rats, Sprague-Dawley; Solubility; Surface Properties; Tumor Cells, Cultured

Sesamin, a polyphenolic compound found in sesame seeds, has been reported to exert a variety of beneficial health effects. We have previously reported that sesamin increases the lifespan of Caenorhabditis elegans. In this study, we investigated the molecular mechanisms underlying the longevity effect of sesamin in C. elegans.. Starting from three days of age, Caenorhabditis elegans animals were fed a standard diet alone or supplemented with sesamin. A C. elegans genome array was used to perform a comprehensive expression analysis. Genes that showed differential expression were validated using real-time PCR. Mutant or RNAi-treated animals were fed sesamin, and the lifespan was determined to identify the genes involved in the longevity effects of sesamin.. The microarray analysis revealed that endoplasmic reticulum unfolded protein response-related genes, which have been reported to show decreased expression under conditions of SIR-2.1/Sirtuin 1 (SIRT1) overexpression, were downregulated in animals supplemented with sesamin. Sesamin failed to extend the lifespan of sir-2.1 knockdown animals and of sir-2.1 loss-of-function mutants. Sesamin was also ineffective in bec-1 RNAi-treated animals; bec-1 is a key regulator of autophagy, and is necessary for longevity induced by sir-2.1 overexpression. Furthermore, the heterozygotic mutation of daf-15, which encodes the target of rapamycin (TOR)-binding partner Raptor, abolished lifespan extension by sesamin. Moreover, sesamin did not prolong the lifespan of loss-of-function mutants of aak-2, which encodes the AMP-activated protein kinase (AMPK).. Sesamin extends the lifespan of C. elegans through several dietary restriction-related signaling pathways, including processes requiring SIRT1, TOR, and AMPK.

Topics: AMP-Activated Protein Kinases; Animals; Antioxidants; Caenorhabditis elegans; Caenorhabditis elegans Proteins; Caloric Restriction; Dietary Supplements; Dioxoles; Food Additives; gamma-Cyclodextrins; Gene Expression Profiling; Gene Expression Regulation, Developmental; Gene Knockdown Techniques; Intrinsically Disordered Proteins; Lignans; Mutation; Oligonucleotide Array Sequence Analysis; RNA Interference; Sirtuins; Survival Analysis; TOR Serine-Threonine Kinases

Nutritional control has been proposed as a potential therapy for slowing the senescence of immune function and decreasing mortality. This study investigated whether sesamin could modify host defense systems and extend the lifespan of the nematode Caenorhabditis elegans.. Nematodes were fed standard food (the bacterium Escherichia coli strain OP50) supplemented with various doses of sesamin/γ-cyclodextrin inclusion compounds starting from young adulthood. The mean lifespan, muscle function, lipofuscin accumulation, protein carbonyl content, and stress resistance of the worms were examined. Then, C. elegans mutants harboring loss-of-function lesions in longevity- and host defense-related signaling pathways were supplemented with sesamin to identify the genes involved in the longevity effects.. Worms supplemented with sesamin displayed higher locomotion and prolongevity and produced offspring at levels similar to unsupplemented control animals. The growth curves of nematodes were similar to those of controls, suggesting that sesamin did not induce prolongevity effects through dietary restriction. Notably, sesamin made the worms more resistant to infection by Legionella pneumophila and more resistant to oxidative stressors such as paraquat and hydrogen peroxide and prolonged the lifespan of a mev-1 mutant that produces abundant superoxide anions. However, the accumulation of protein carbonyls and lipofuscin was similar in sesamin-exposed and control worms, suggesting that sesamin is unlikely to work simply as an antioxidant. Sesamin supplementation failed to extend the lifespan of loss-of-function mutants of daf-2, daf-16, pmk-1, and skn-1.. Sesamin enhances the host defense of C. elegans and increases the average lifespan via activation of both skn-1 (encoding a component of the p38 MAPK pathway) and daf-16 (encoding a component of the IGF-1 pathway).

Topics: Administration, Oral; Animals; Antioxidants; Caenorhabditis elegans; Dioxoles; Escherichia coli; gamma-Cyclodextrins; Insulin-Like Growth Factor I; Legionella pneumophila; Lignans; Longevity; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Protein Carbonylation; Salmonella enterica; Signal Transduction